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Vulnerability and Genetic Susceptibility to Cigarette Smoke–Induced Emphysema in Mice
Vulnerability and Genetic Susceptibility to Cigarette Smoke–Induced Emphysema in Mice
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Vulnerability and Genetic Susceptibility to Cigarette Smoke–Induced Emphysema in Mice
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Vulnerability and Genetic Susceptibility to Cigarette Smoke–Induced Emphysema in Mice
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Vulnerability and Genetic Susceptibility to Cigarette Smoke–Induced Emphysema in Mice
Vulnerability and Genetic Susceptibility to Cigarette Smoke–Induced Emphysema in Mice
Journal Article

Vulnerability and Genetic Susceptibility to Cigarette Smoke–Induced Emphysema in Mice

2017
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Overview
Cigarette smoke (CS) has been identified as the most important risk factor for the development of chronic obstructive pulmonary disease (COPD). Studies of cigarette/tobacco smoke-induced COPD have primarily utilized small laboratory animals, particularly inbred laboratory mice, as the model of choice. The first comprehensive review of animal models of emphysema relating to the pathogenesis of COPD was published in 2002 (1), and a more recent review provided updates on this topic (2). The use of this species has several advantages, including a relatively low cost, a rapid reproductive cycle, large litter sizes, and the availability of antibodies and molecular probes developed specifically for mouse research. In addition to the study limitations identified by the authors, only female mice were used, and sex-specific differences may be important (13). Also, the authors were unable to detect any regions that strictly met multiple testing correction thresholds. Importantly, alveolar chord length is not a correlate/measure for emphysema, and emphysema is only one pathological entity of COPD.